Wednesday, July 23, 2008

Possibility Of Cracking Herpes Now Exists

Cold sores and shingles, two forms of the very annoying – and very difficult to deal with – herpes virus may no longer be as difficult to find and flush out as it has been since it was discovered. U.S.-based researchers believe they have managed to found a way to flush out the annoying little virus using a mysterious genetic trait carried by the herpes simplex-1 virus – which causes cold sores in those who are infected by it – that allows it to linger undetected in the nerves that it infects. The herpes virus, according to the research team, manages to remain in stealth mode via the use of microRNAs, small bits of genetic material that allow for the regulation of the activities of many viruses.

According to the researchers, it is possible to force the virus to become active, and then proceed to eliminate it by using standard antiviral medications. One cited example was acyclovir. This information was stated by Jennifer Lin Umbach, from Duke University in North Carolina, who was one of those who worked on the study that obtained the data. Umbach said that the team was trying to go into animal trials to determine the veracity of their assumptions.

Based on news reports, the team from Duke is engaging in discussions for a potential collaborative effort with Regulus Therapeutics LLC, a joint venture between Alnylam Pharmaceuticals, Inc and Isis Pharmaceuticals, Inc. The group is known for specializing in microRNA studies.

The herpes viruses are known for causing many permanent infections, often heading straight to the nerve cells they damage. The ability of the virus to remain dormant in the life of any given host – animal or human – can often cause periodic outbreaks to occur when the virus begins to awaken. Herpes simplex-1 causes cold sores, herpes simplex 2 causes genital herpes, and varicella can cause chicken pox in younger patients. For older patients, varicella can appear as herpes zoster, the cause of shingles. Anti-viral medications have only been known to slow the progress of the virus down, not remove it from the body outright.

The main problem I’ve seen in texts about herpes is that it can’t be killed with any treatment available if the bug is still inactive. Without the virus being active and causing damage, it simply can’t be treated or stopped. Another interesting trait of the condition is that the same virus can end up infecting different neurons in the same body, and were also able to activate the infections at different times. These two combined traits make it difficult – if not outright impossible – to wipe out an infection in a single person, let alone a widespread and dormant one. This means that discovering the gene that controls the microRNAs that trigger the active stage of the virus can go a long way in helping medical science counter the threat of herpes.

However, for the time being, this is all strictly conjecture at this point. There’s still no direct evidence saying that it would be possible to activate those genetic markers, let alone be able to activate them reliably. Still, this is currently the best lead medical science has to finding a cure for herpes, so not everything is bad.


Resource Box : Harvey Ong is currently employed as a researcher for an online media company, currently writing about pharmaceutical products and herbal remedies. He is also an amateur paleontologist and has a collection of various animal toxins, for research reasons.

Sunday, July 6, 2008

Protein-Alzheimer’s Link Being Probed

Alzheimer’s. People know it. People fear it.

Unfortunately, people can’t cure it, either.

The sad part is that nobody seems to have any idea what causes this problem. There are numerous scattered theories that suggest one thing or another, but really, the medical community knows very little about the causes of this. Which sort of makes it a disease that’s exceedingly tough to cure, doesn’t it? After all, if you don’t know what’s causing a problem, you’re sort of stuck playing damage control for the effects. You can’t really solve it without knowing what the root of it is. This is, presumably, why there are so many studies going on that are trying to find out what makes Alzheimer’s tick. Once we know what causes it, maybe we can find a way to reverse the damage? Or maybe even prevent it from happening. A bit of a dream, so for now, we stick with treatment.

Well, there might be some hope along that horizon. A research team believes that they may have found a sticky little protein that could be linked to the condition. They’ve found that they caused symptoms of memory loss similar to a number of forms of dementia in rats by injecting a protein they call beta-amyloid. According to them, this protein is also present in patients with Alzheimer’s. Apparently, it forms some sort of plague-like problem that can be found in the brains of people with the aforementioned condition. Nobody’s really been able to tell whether this was the cause or just one of the side effects, though. After all, the problem shows up in people without Alzheimer’s.

Tests have been done on this protein before, I’m told. This is because, as stated, it does tend to show up in patients with Alzheimer’s. Many believed that it might have held some sort of connection to the cause of the disease. Some believed that the discovery of the protein in people without the condition negated that hypothesis, but this latest revelation is proving promising in reviving beta-amyloid as a potential avenue of research. And in the quest to find out what triggers Alzheimer’s – and how to fix the damage so that the trigger can be undone – then any given lead is as good as anything.

It should be made known that there are basically three types of the aforementioned protein. Each of them is, clearly, of the sticky variety. Each one is generally found in patients with Alzheimer’s, and in some cases, in people who don’t have the condition and have no signs of developing any form of dementia. According to the research team, the first two types did not cause any sort of dementia in the laboratory test subjects that were injected with it. Whether or not this disproves the connection with dementia is unknown. The third type of the protein, in contrast, definitely caused some effect. Most of the test rats that were injected with it developed dementia.

The question now, however, is why did this happen? And furthermore, can it be prevented?


Resource Box : Harvey Ong is currently working as a writer-researcher for an online pharmaceutical company. He has also had experience field testing blackjack betting systems and is an amateur poker player.




Protein-Alzheimer’s Link Being Probed

Alzheimer’s. People know it. People fear it.

Unfortunately, people can’t cure it, either.

The sad part is that nobody seems to have any idea what causes this problem. There are numerous scattered theories that suggest one thing or another, but really, the medical community knows very little about the causes of this. Which sort of makes it a disease that’s exceedingly tough to cure, doesn’t it? After all, if you don’t know what’s causing a problem, you’re sort of stuck playing damage control for the effects. You can’t really solve it without knowing what the root of it is. This is, presumably, why there are so many studies going on that are trying to find out what makes Alzheimer’s tick. Once we know what causes it, maybe we can find a way to reverse the damage? Or maybe even prevent it from happening. A bit of a dream, so for now, we stick with treatment.

Well, there might be some hope along that horizon. A research team believes that they may have found a sticky little protein that could be linked to the condition. They’ve found that they caused symptoms of memory loss similar to a number of forms of dementia in rats by injecting a protein they call beta-amyloid. According to them, this protein is also present in patients with Alzheimer’s. Apparently, it forms some sort of plague-like problem that can be found in the brains of people with the aforementioned condition. Nobody’s really been able to tell whether this was the cause or just one of the side effects, though. After all, the problem shows up in people without Alzheimer’s.

Tests have been done on this protein before, I’m told. This is because, as stated, it does tend to show up in patients with Alzheimer’s. Many believed that it might have held some sort of connection to the cause of the disease. Some believed that the discovery of the protein in people without the condition negated that hypothesis, but this latest revelation is proving promising in reviving beta-amyloid as a potential avenue of research. And in the quest to find out what triggers Alzheimer’s – and how to fix the damage so that the trigger can be undone – then any given lead is as good as anything.

It should be made known that there are basically three types of the aforementioned protein. Each of them is, clearly, of the sticky variety. Each one is generally found in patients with Alzheimer’s, and in some cases, in people who don’t have the condition and have no signs of developing any form of dementia. According to the research team, the first two types did not cause any sort of dementia in the laboratory test subjects that were injected with it. Whether or not this disproves the connection with dementia is unknown. The third type of the protein, in contrast, definitely caused some effect. Most of the test rats that were injected with it developed dementia.

The question now, however, is why did this happen? And furthermore, can it be prevented?


Resource Box : Harvey Ong is currently working as a writer-researcher for an online pharmaceutical company. He has also had experience field testing blackjack betting systems and is an amateur poker player.